Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Imaging the ageing musculoskeletal system
How long is a generation? This is a debate that simmers in the disciplines of anthropology, genetics and genealogy. Generations can be very short, with both males and females becoming parents in their early teens, or very long, with men fathering children in their 10th decade, but these variations are uncommon. It is probable that the average male generation is somewhere between 30 and 35 years and that female generations are shorter, at between 25 and 30 years. Despite a long-held assumption that generations were shorter in prehistoric societies there is now evidence to suggest that these mean generational gaps have been stable for millennia ( ).
For genealogists these figures are used as a rule of thumb to assess the integrity of a family tree. Too few generations in a given century alerts them to the possibility of missing data. For geneticists these figures are used to estimate the rate at which mutations have occurred in our genome. And in evolutionary terms these figures may determine the age at which our bodies begin to fail.
It seems reasonable to argue that the child of a parent who remains healthy, until their offspring are independent, is more likely to survive and propagate their genes than the progeny of a weak and feeble parent. The traits of good health in parenthood would therefore be passed on to subsequent generations whereas the weaker phenotype would be less likely to endure. Assuming that the age of independence is 15, then the evolutionary driver is a parent who is healthy until the age of 45. After that a healthy parent is much less likely to contribute to the survival of the offspring; evolution has selected a human phenotype that remains strong until the age of 45 and then starts to fall apart.
While the estimate of intervals between generations has an evidence base, my subsequent argument is a hypothesis. One that is supported by a number of facts: at 45 we go grey ( ), we become short sighted ( ) and we suffer a peak in short-term musculoskeletal pain ( ). At age 45 the production of new collagen in cartilage and bone falls to the lowest level in our lifetimes ( ) and we start to shrink ( ).
Cartilage
Normal hyaline cartilage in a young adult has a laminar appearance on magnetic resonance (MR) imaging ( Fig. I.3.1 ). The vertical and oblique zones of type 1 collagen fibres that make up the parabolic arcades of Benninghoff ( ), and the armour-plated surface layer can be differentiated because the orientation of collagen fibres influences the signal generated by radiofrequency pulses. The extracellular matrix of cartilage, consisting mainly of glycosaminoglycan, is hygroscopic; as water is absorbed the cartilage expands until limited by the collagen arcades. This balanced tension between expanding extracellular matrix and restraining collagen is often referred to as a hydrostatic cushion, implying that hyaline articular cartilage plays a significant role in load distribution. As we shall see later this may not be the case, and the main role of hydrostatic cartilage may be to resist shearing forces.
As we age, our chondrocytes die. Those that survive synthesize less glycosaminoglycan which means that less water is bound into the cartilage, which gets thinner and loses its compressive stiffness ( ). This age-related biological degeneration is commonly seen in routine clinical practice ( Fig. I.3.1 ) where, paradoxically, many musculoskeletal radiologists will resist describing them as degenerative. This is because in clinical practice the terms ‘degeneration’ and ‘osteoarthritis’ are often used interchangeably. An alternative approach is to describe uncomplicated thinning of articular cartilage as normal age-related change, the assumption being that this does not contribute to symptoms. Once the integrity of the articular cartilage has been breached, or there is reactive subchondral bone marrow signal, this may then be described as being ‘degenerative’. When the clinical history or secondary signs of inflammation support the diagnosis, then these findings can be interpreted as ‘osteoarthritis’.
All these assumptions and tortuous semantic manipulations illustrate one of the principal difficulties that clinicians and scientists have when approaching the ageing musculoskeletal system. We do not have a language that allows us to differentiate normal ageing from degenerative disease and the imaging phenotypes do not allow us to separate the two with any certainty.
For the purpose of clinical practice most clinicians consider diffuse thinning of articular cartilage to be a predictable asymptomatic feature of the ageing musculoskeletal system. This does not mean that it is entirely benign. The thin, soft and collagen-depleted cartilage is less resistant to shearing injuries and is therefore a risk factor for developing osteoarthritis (OA). The knee joint in particular is dependent on the integrity of the cruciate and collateral ligaments, rather than the profile of the articular surfaces, for its stability. As the joint space narrows so these ligaments become redundant and the joint becomes intrinsically less stable; there is a view that the redundancy of stabilizing ligaments caused by joint space narrowing is a significant source of symptoms ( ).
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here
